After a small vessel is ruptured, which immediate response reflects intrinsic smooth muscle contraction of the vessel wall itself?

A. Endothelial budding
B. Fibrin polymerization
C. Myogenic spasm
D. Leukocyte rolling

C. Myogenic spasm

Damaged tissue can promote early postinjury vasoconstriction through locally released:

A. Autacoid factors
B. Fibrin monomers
C. Plasmin fragments
D. Acute phase proteins

A. Autacoid factors

Which mechanism represents a contribution to immediate vasoconstriction after vascular injury?

A. Collagen exposure
B. Platelet degranulation
C. Fibrin cross-linking
D. Nervous reflexes

D. Nervous reflexes

Ongoing platelet activity helps narrow a recently injured vessel by releasing:

A. Fibrinopeptide B
B. Thromboxane A2
C. Protein C
D. Tissue plasminogen

B. Thromboxane A2

A superficial capillary nick stops bleeding before a stable fibrin mesh develops. The defect was most likely sealed initially by a:

A. Platelet plug
B. Fibrin reticulum
C. Fibroblast scar
D. Red cell cast

A. Platelet plug

Circulating thrombocytes arise from fragmentation of:

A. Myeloblasts
B. Hepatocytes
C. Megakaryocytes
D. Endothelial cells

C. Megakaryocytes

Which platelet contractile protein is most directly involved in clot contraction?

A. Talin
B. Spectrin
C. Fibrillin
D. Thrombosthenin

D. Thrombosthenin

After endothelial denudation, platelets adhere most directly to exposed:

A. Collagen and fibrin
B. Collagen and vWF
C. Elastin and albumin
D. Laminin and plasmin

B. Collagen and vWF

Platelet surface glycoproteins participate in adhesion by binding:

A. von Willebrand factor
B. Tissue factor
C. Antithrombin III
D. High-molecular kininogen

A. von Willebrand factor

Early during platelet aggregation, activated platelets release:

A. Protein C and S
B. Heparin and plasmin
C. ADP and PAF
D. Fibrin and factor XIII

C. ADP and PAF

Which group most directly amplifies recruitment of nearby platelets at an injury site?

A. Factor XII, prekallikrein, HMWK
B. Thrombin, protein C, plasmin
C. Serotonin, albumin, fibrin
D. ADP, PAF, TXA2

D. ADP, PAF, TXA2

A thrombocytopenic patient develops multiple pinpoint hemorrhages under the skin. These lesions are termed:

A. Ecchymoses
B. Petechiae
C. Telangiectasias
D. Hematomas

B. Petechiae

A formed clot that becomes organized during healing is most likely to undergo:

A. Invasion by fibroblasts
B. Hyaline degeneration
C. Neutrophilic cavitation
D. Endothelial exfoliation

A. Invasion by fibroblasts

A small clot that disappears rather than becoming organized has most likely undergone:

A. Ossification
B. Encapsulation
C. Fatty change
D. Dissolution

D. Dissolution

The first general step in coagulation is:

A. Fibrin cross-linking
B. Prothrombin activator formation
C. Platelet plug retraction
D. Plasmin generation

B. Prothrombin activator formation

The second general step of coagulation is best described as:

A. Factor XIII activation
B. Fibrin stabilization
C. Prothrombin to thrombin
D. Plasminogen to plasmin

C. Prothrombin to thrombin

The final general step in clot formation is:

A. Fibrinogen to fibrin
B. Factor X to Xa
C. Platelet adhesion to collagen
D. Prothrombin synthesis

A. Fibrinogen to fibrin

Factor Xa most directly converts prothrombin to thrombin in the presence of sufficient:

A. ADP
B. vWF
C. Fibrinogen
D. Ca2+

D. Ca2+

The rate-limiting event in blood coagulation is the formation of:

A. Thrombin
B. Fibrin monomers
C. Prothrombin activator
D. Cross-linked fibrin

C. Prothrombin activator

Prothrombin is synthesized primarily in the:

A. Spleen
B. Liver
C. Bone marrow
D. Vascular endothelium

B. Liver

A patient with impaired vitamin-dependent hepatic clotting function would have defective normal activation of prothrombin because the liver requires vitamin:

A. K
B. C
C. B6
D. E

A. K

Fibrinogen is synthesized primarily in the:

A. Spleen
B. Platelet granules
C. Bone marrow
D. Liver

A. Spleen

In coagulation, thrombin functions primarily as a:

A. Carrier protein
B. Protease
C. Kinase
D. Phosphatase

B. Protease

Once fibrin strands are formed, the reticulum is strengthened by:

A. Thromboxane A2
B. Platelet factor 4
C. Fibrin stabilizing factor
D. Tissue factor inhibitor

C. Fibrin stabilizing factor

A laboratory specimen forms a clot but fails to retract appropriately. This finding most strongly suggests decreased:

A. Circulating platelets
B. Vitamin K stores
C. Hepatic fibrinogen
D. Plasma calcium

A. Circulating platelets

In this material, fibrin stabilizing factor is released by:

A. Hepatocytes
B. Neutrophils
C. Endothelium
D. Platelets

D. Platelets

Thrombin exerts what effect on its own generation?

A. No meaningful feedback
B. Positive feedback
C. Negative feedback
D. Delayed inhibition

B. Positive feedback

A patient with extensive soft-tissue trauma develops rapid coagulation through the pathway initiated outside the bloodstream. Which pathway is most directly involved?

A. Common pathway
B. Intrinsic pathway
C. Extrinsic pathway
D. Fibrinolytic pathway

C. Extrinsic pathway

In contrast to the extrinsic pathway, the intrinsic pathway is best characterized by which initiating feature?

A. Begins in the blood
B. Starts in the liver
C. Requires fibrinolysis first
D. Needs mast cell rupture

A. Begins in the blood

A crush injury to skeletal muscle rapidly activates coagulation because trauma to the vascular wall and surrounding tissues preferentially triggers the:

A. Protein C pathway
B. Extrinsic pathway
C. Intrinsic pathway
D. Plasmin pathway

B. Extrinsic pathway

The first major event in the extrinsic pathway is release of:

A. Prekallikrein
B. Platelet factor 4
C. Tissue factor
D. Factor VIII

C. Tissue factor

Traumatized tissue releases which substance to initiate the extrinsic cascade?

A. Thromboplastin
B. Plasminogen
C. Thrombomodulin
D. Antithrombin III

A. Thromboplastin

In the extrinsic pathway, tissue factor complexes with which factor before activation of factor X?

A. Factor V
B. Factor VII
C. Factor IX
D. Factor XI

B. Factor VII

In tissue injury, factor X is most directly converted to Xa by the combination of:

A. VIIIa and IXa
B. XIIa and XIa
C. V and calcium
D. VII and tissue factor

D. VII and tissue factor

Which event occurs immediately after factor X activation in the extrinsic pathway?

A. Fibrin degradation
B. Prothrombin synthesis
C. Xa forms prothrombin activator
D. XI converts to XIa

C. Xa forms prothrombin activator

In the extrinsic pathway, prothrombin is split to thrombin in the presence of:

A. HMW kininogen
B. Platelet factor 3
C. Calcium
D. Oxalate

C. Calcium

Which factor accelerates protease activity in the extrinsic pathway and promotes more clotting by positive feedback?

A. Factor II
B. Factor V
C. Factor VIII
D. Factor XII

B. Factor V

A coagulation defect selectively impairing the accelerating factor of the extrinsic pathway would most directly involve:

A. Factor V
B. Factor VII
C. Factor IX
D. Factor XIII

A. Factor V

A researcher compares clotting pathways and notes one is triggered by trauma to blood itself or exposure of blood to collagen. This describes the:

A. Extrinsic pathway
B. Fibrinolytic pathway
C. Intrinsic pathway
D. Protein C pathway

C. Intrinsic pathway

Exposure of blood to subendothelial collagen most directly instigates the:

A. Extrinsic pathway
B. Intrinsic pathway
C. Common pathway only
D. Plasmin pathway

B. Intrinsic pathway

The earliest intrinsic-pathway event after blood trauma is activation of factor XII along with release of:

A. Protein C
B. Platelet phospholipids
C. Antithrombin III
D. Tissue factor

B. Platelet phospholipids

When blood trauma occurs, platelet phospholipids release:

A. PF3
B. PGI2
C. t-PA
D. vWF

A. PF3

In the intrinsic pathway, factor XIIa converts factor XI to XIa only in the presence of:

A. Tissue factor
B. Antithrombin III
C. HMW kininogen
D. Protein S

C. HMW kininogen

Which substance accelerates the conversion of factor XI to XIa during intrinsic coagulation?

A. Citrate
B. Prekallikrein
C. Oxalate
D. Thrombomodulin

B. Prekallikrein

In the intrinsic pathway, factor XIa most directly converts:

A. VIII to VIIIa
B. X to Xa
C. IX to IXa
D. II to IIa

C. IX to IXa

Activation of factor X through the intrinsic pathway requires IXa acting together with VIIIa, platelet phospholipids, and:

A. Factor III
B. Factor VII
C. Factor XII
D. Protein C

A. Factor III

Which combination is required for intrinsic activation of factor X?

A. VIIa, tissue factor, calcium
B. XIIa, XIa, prekallikrein
C. IXa, VIIIa, III, phospholipids
D. V, thrombin, antithrombin III

C. IXa, VIIIa, III, phospholipids

After factor X becomes Xa in the intrinsic pathway, Xa forms prothrombin activator with assistance from:

A. Factor V
B. Factor VII
C. Factor VIII
D. Factor XIII

A. Factor V

Following formation of prothrombin activator in the intrinsic pathway, the next step is:

A. XI to XIa
B. Prothrombin to thrombin
C. Fibrin to plasmin
D. VIII to VIIIa

B. Prothrombin to thrombin

The final step listed in the intrinsic pathway is conversion of:

A. Thrombin to prothrombin
B. Fibrin to fibrinogen
C. Fibrinogen to fibrin
D. Plasminogen to plasmin

C. Fibrinogen to fibrin

Compared with the extrinsic pathway, the intrinsic pathway generally occurs:

A. Faster
B. Slower
C. Simultaneously
D. Independently

B. Slower

Contact of factor XII and platelets with collagen most directly initiates the:

A. Extrinsic pathway
B. Intrinsic pathway
C. Common pathway
D. Protein C pathway

B. Intrinsic pathway

A phlebotomy specimen is prevented from clotting by chemically reducing ionized calcium. Which additive could achieve this?

A. Heparin only
B. Nitric oxide
C. Citrate
D. Tissue factor

C. Citrate

Which additive also prevents clotting in removed blood by reducing available calcium?

A. Oxalate
B. PGI2
C. Protein C
D. PF3

A. Oxalate

Which endothelial property normally helps prevent contact activation of the intrinsic clotting system?

A. Surface smoothness
B. Tissue factor exposure
C. Mast cell heparin
D. Fibrin polymerization

A. Surface smoothness

The endothelial glycocalyx helps prevent coagulation primarily by:

A. Activating factor XII
B. Repelling clotting factors
C. Releasing tissue factor
D. Converting plasminogen

B. Repelling clotting factors

Which endothelial membrane-bound molecule contributes to prevention of clotting in normal vessels?

A. Thrombomodulin
B. Thrombosthenin
C. Thromboplastin
D. PF3

A. Thrombomodulin

Thrombomodulin bound to thrombin most directly activates:

A. Protein C
B. Factor V
C. Factor X
D. Plasmin

A. Protein C

Activated protein C exerts anticoagulant effects by inactivating which factors?

A. II and VII
B. V and VIII
C. IX and X
D. XI and XII

B. V and VIII

Two prominent endothelial vasodilators that inhibit platelet aggregation are:

A. NO and PGI2
B. ADP and PAF
C. TXA2 and serotonin
D. t-PA and plasmin

A. NO and PGI2

Which prostanoid released by endothelium inhibits platelet aggregation?

A. TXA2
B. PGI2
C. PGE1
D. PGF2α

B. PGI2

An important circulating anticoagulant that removes thrombin from blood is:

A. Protein C
B. Fibrinogen
C. Antithrombin III
D. vWF

C. Antithrombin III

Besides antithrombin III, which structure in a developing clot can help remove thrombin?

A. Fibrin fibers
B. Platelet glycocalyx
C. Tissue factor
D. Factor VIIIa

A. Fibrin fibers

Heparin exerts its major anticoagulant effect in this material by binding to antithrombin III and increasing removal of:

A. Fibrinogen
B. Thrombin
C. Protein C
D. Tissue factor

B. Thrombin

Heparin bound to antithrombin III inactivates which activated clotting-factor range?

A. IIa–V
B. Va–VIIIa
C. IXa–XIIa
D. I–IV

C. IXa–XIIa

A hospitalized patient receives heparin. Its anticoagulant action is enhanced because heparin is working with:

A. Tissue factor
B. Antithrombin III
C. Factor V
D. Prekallikrein

B. Antithrombin III

Heparin is released primarily by:

A. Neutrophils
B. Hepatocytes
C. Mast cells
D. Megakaryocytes

C. Mast cells

Which enzyme digests fibrin and also degrades fibrinogen, factor V, factor VIII, prothrombin, and factor XII?

A. Thrombin
B. Plasmin
C. Kallikrein
D. Elastase

B. Plasmin

Conversion of plasminogen to plasmin is catalyzed by:

A. PF3
B. Antithrombin III
C. t-PA
D. Protein C

C. t-PA

A patient receives thrombolytic therapy for an acute clot. The drug most directly mimics the action of:

A. Tissue plasminogen activator
B. Factor V accelerator
C. Platelet factor 3
D. HMW kininogen

A. Tissue plasminogen activator

One of the classic major causes of excessive bleeding?

A. Hemophilia
B. Thrombosis
C. Polycythemia
D. Vasculitis

A. Hemophilia

A malnourished patient with prolonged coagulation studies has excessive bleeding due to deficiency of which factor-related nutrient?

A. Vitamin K
B. Vitamin C
C. Vitamin D
D. Vitamin B12

A. Vitamin K

A patient with diffuse petechiae and a markedly decreased platelet count has excessive bleeding due to:

A. Hemophilia
B. Hypercoagulability
C. Vitamin K deficiency
D. Thrombocytopenia

D. Thrombocytopenia

Vitamin K serves as a cofactor for which hepatic enzyme type?

A. Protease
B. Carboxylase
C. Oxidase
D. Transferase

B. Carboxylase

Vitamin K–dependent carboxylation directly modifies which clotting factor?

A. Factor VIII
B. Factor II
C. Factor XI
D. Factor XII

B. Factor II

Which clotting factor also requires vitamin K–dependent carboxylation in the liver?

A. Factor VIII
B. Factor V
C. Factor XIII
D. Factor VII

D. Factor VII

A defect in vitamin K–dependent carboxylation would impair activation of which additional factor?

A. Factor IX
B. Factor VIII
C. Factor XI
D. Factor XII

A. Factor IX

Vitamin K deficiency would also reduce proper hepatic modification of:

A. Factor XI
B. Factor XII
C. Factor X
D. Factor VIII

C. Factor X

Which anticoagulant protein is included among the vitamin K–dependent carboxylated proteins?

A. Protein C
B. Protein S
C. Plasmin
D. Antithrombin III

A. Protein C

Vitamin K is recycled back to its active form by:

A. Cyclooxygenase
B. Thrombin
C. t-PA
D. VKORC1

D. VKORC1

Hemophilia occurs almost exclusively in:

A. Males
B. Females
C. Neonates
D. Elderly patients

A. Males

Most cases of hemophilia are caused by deficiency of:

A. Factor IX
B. Factor XI
C. Factor X
D. Factor VIII

D. Factor VIII

A patient with the less common classic hemophilia variant has deficiency of:

A. Factor VIII
B. Factor IX
C. Factor VII
D. Factor V

B. Factor IX

Deficiency of factor IX is specifically termed:

A. von Willebrand disease
B. Hemophilia A
C. DIC
D. Hemophilia B

D. Hemophilia B

In hemophilia A, the primarily affected coagulation pathway is the:

A. Extrinsic pathway
B. Common pathway
C. Intrinsic pathway
D. Fibrinolytic pathway

C. Intrinsic pathway

Loss of the larger component of factor VIII produces:

A. Hemophilia B
B. DIC
C. ITP
D. von Willebrand disease

D. von Willebrand disease

A patient develops thrombocytopenia after an infiltrative infectious process involving the marrow. Which mechanism best explains the low platelet count?

A. Bone marrow infection
B. Splenic sequestration
C. Platelet consumption
D. Dilutional loss

A. Bone marrow infection

A patient with autoimmune platelet destruction has thrombocytopenia due to:

A. Portal hypertension
B. Transfusion dilution
C. Marrow infection
D. Antibody-mediated destruction

D. Antibody-mediated destruction

A cirrhotic patient with portal hypertension has thrombocytopenia mainly because of:

A. Marrow suppression
B. Splenic sequestration
C. Platelet dilution
D. Protein C deficiency

B. Splenic sequestration

Widespread microvascular clotting may lower platelet count through:

A. Decreased thrombopoiesis
B. Splenic rupture
C. Platelet consumption in thrombi
D. Increased platelet turnover

C. Platelet consumption in thrombi

A massively transfused trauma patient develops low platelets primarily because of:

A. Dilution from transfusion
B. Platelet autoantibodies
C. Marrow infection
D. Portal congestion

A. Dilution from transfusion

In selected patients with thrombocytopenia, which intervention may be beneficial?

A. Hepatectomy
B. Splenectomy
C. Nephrectomy
D. Appendectomy

B. Splenectomy

An abnormal clot forming within an intact blood vessel is called a:

A. Embolus
B. Hematoma
C. Petechia
D. Thrombus

D. Thrombus

A detached intravascular clot traveling in the circulation is a:

A. Embolus
B. Purpura
C. Thrombus
D. Fibrin strand

A. Embolus

A lower-extremity clot that dislodges and obstructs the pulmonary arteries causes:

A. Cerebral embolism
B. Pulmonary embolism
C. Coronary thrombosis
D. Portal embolism

B. Pulmonary embolism

Septicemia may trigger simultaneous diffuse coagulation and consumption known as:

A. TTP
B. HIT
C. ITP
D. DIC

D. DIC

Warfarin therapy lowers levels of which vitamin K–dependent factor?

A. Factor IX
B. Factor VIII
C. Factor XII
D. Factor XI

A. Factor IX

Coumarin therapy also decreases which factor most associated with the extrinsic pathway?

A. Factor VIII
B. Factor IX
C. Protein C
D. Factor VII

D. Factor VII

Warfarin lowers which precursor listed in this material?

A. Active prothrombin
B. Fibrinogen
C. Plasminogen
D. Factor VIII

A. Active prothrombin

Which additional factor falls with warfarin use?

A. Factor V
B. Factor X
C. Factor XI
D. Factor XIII

B. Factor X

Warfarin most directly inhibits which enzyme?

A. Thrombin
B. Factor Xa
C. VKORC1
D. Cyclooxygenase

C. VKORC1

Exposure of blood to silicon inactivates platelets and:

A. Factor IX
B. Factor XI
C. Factor X
D. Factor XII

D. Factor XII

Removal of ionized calcium from blood will produce:

A. More coagulation
B. Faster fibrinolysis
C. Less coagulation
D. Platelet activation

C. Less coagulation

Bleeding time most directly evaluates:

A. Platelet levels
B. Extrinsic pathway
C. Intrinsic pathway
D. Fibrin stability

A. Platelet levels

Prothrombin time is primarily used to evaluate the:

A. Intrinsic pathway
B. Common pathway
C. Platelet system
D. Extrinsic pathway

D. Extrinsic pathway

The normal INR range given in this material is:

A. 2.0 to 3.0
B. 0.9 to 1.3
C. 1.5 to 2.5
D. 3.0 to 4.0

B. 0.9 to 1.3

A markedly elevated INR most strongly indicates:

A. Risk of bleeding
B. Platelet deficiency
C. Faster clot retraction
D. Hyperfibrinolysis

A. Risk of bleeding

A low INR most strongly suggests:

A. Factor VIII deficiency
B. Hepatic failure
C. Vitamin K deficiency
D. High chance of clot

D. High chance of clot

A patient appropriately anticoagulated with warfarin should generally have an INR of:

A. 2.0 to 3.0
B. 0.9 to 1.3
C. 1.2 to 1.8
D. 3.5 to 4.5

A. 2.0 to 3.0

Classic hemophilia differs from von Willebrand disease in this material because classic hemophilia reflects loss of the:

A. Larger VIII component
B. vWF-binding domain
C. Smaller VIII component
D. Platelet membrane receptor

C. Smaller VIII component